Normal values and upper limits (95th percentile) of liver, spleen, pancreas, and portal vein size were determined prospectively with ultrasound in 915 healthy subjects. Sex, age, weight, height, and body surface area were determined in each case. Since correlation of longitudinal and transverse organ diameters with physical data was poor (r less than or equal to 0.3), the authors do not consider it necessary to correct the measurements accordingly. However, the liver is oriented longitudinally in slender subjects and transversely in heavy subjects; thus both longitudinal and anteroposterior diameters need to be measured, since the longitudinal diameter alone will give too high or too low a value, respectively.

To determine the average diameter and the upper normal limit of the common bile duct in healthy man, 830 blood donors were examined by ultrasound. The mean diameter was 2.5 +/- 1.1 mm (SD) at the porta hepatis and 2.8 +/- 1.2 mm (SD) at the widest point, the regression coefficient between both diameters being r = 0.84. None of the healthy subjects had a diameter larger than 7 mm at any site, and in 95% of all subjects the diameters were less than 4 mm at both sites of measurement. The diameters were significantly correlated with age (r = 0.16) and weight (r = 0.11), but not with sex, height, and body surface area. In 73 patients with cholelithiasis and in 55 patients after cholecystectomy, all of whom lacked clinical or laboratory signs of biliary obstruction, the average diameters at the porta hepatis were 3.8 +/- 2.0 mm and 5.2 +/- 2.3 mm, and at the widest point 4.8 +/- 2.2 mm and 6.2 +/- 2.5 mm, respectively. It is concluded that a common bile duct with any sonographic diameter larger than 4 mm should be followed closely and evaluated further with clinical examinations such as intravenous cholangiography unless cholecystectomy has been performed.

In 43 normolipidemic postmenopausal women we studied fasting and postprandial (oral fat load with 50 g fat per square meter; blood sampling for 5 h) lipoprotein components and lipoprotein(a) levels before and with the administration of conjugated equine estrogens opposed by medrogestone (on days 11-21). Data was compared intraindividually; the second testing was performed during the last 5 days of the combined estrogen/progestogen phase of the third cycle. Fasting low-density lipoprotein (LDL) and total cholesterol concentrations decreased significantly; high-density lipoprotein (HDL) cholesterol, including subfractions HDL2 and HDL3, was not changed. Fasting triglyceride concentrations increased. All lipoprotein fractions measured showed a postprandial elevation with the exception of chylomicron cholesterol concentrations. There was a significant effect of hormone replacement therapy on the postprandial course of total cholesterol (decrease; P < 0.001), VLDL cholesterol (increase; P = 0.025), and the triglyceride proportion in the LDL plus HDL fraction (increase; P < 0.001). With hormone replacement therapy the postprandial curve of total triglycerides was increased only 1 h after the fat load while chylomicron triglyceride concentrations were lowered after 5 h. VLDL triglycerides were not influenced. In all patients with lipoprotein(a) levels above 10 mg/dl, this parameter decreased (about 25%). Although increasing fasting triglyceride concentrations, hormone replacement therapy does not bring about an exaggerated postprandial increase in triglycerides. Postprandial chylomicron clearance is evidently promoted. Hormone replacement therapy leads to a small increase in triglycerides in the LDL plus HDL fraction by inhibiting hepatic lipase activity. Moreover, the decrease in lipoprotein(a) levels may contribute to the antiatherosclerotic effect.

SUMMARY Provided the intragastric pH is greater than 6 and the collected gastric juice is boiled and neutralised immediately, considerable amounts of gastrin-like immunoreactivity can be found in human gastric juice. Characterisation according to size and charge reveals that nearly all the gastrin-like immunoreactivity is similar to gastrin 1-17. Direct stimulation of the G-cells with protein solution is followed by a significant and simultaneous increase of acid secretion, serum gastrin, and gastrin output into the lumen of the stomach in control subjects and patients with duodenal ulcer. consecutive 15 minute periods with 50 ml 10% peptone pH 7.0 (540 mosm/kg, Difco Laboratories, Detroit, Michigan, USA). The perfusate entered the stomach via the tube positioned in the gastric fundus and was collected via the antral catheter in a glass cylinder standing in a boiling water bath. The gastric juice was immediately neutralised by addition of 0.1 N sodium hydroxide. Before neutralisation, the pH of the gastric juice was recorded. Acid secretion per 15 minute sample was determined. Aliquots of venous blood were taken at the end of each collection period. Serum and gastric juice samples were frozen after collection and treatment and stored at -200C.In five healthy volunteers and five patients with duodenal ulcer the stomach was perfused in the same way with 0.42 M sodium bicarbonate adjusted to pH 5.5 with 1 N hydrochloric acid (825 mosm/kg) and 20% peptone pH 5-5 (1080 mosm/kg). The recovered perfusates were treated as described above.To exclude G-cell damage caused by phosphate buffer, the stomach of four control persons and four duodenal ulcer patients was alternately perfused for six consecutive 15 minute periods with 0-6 M sodium bicarbonate adjusted to pH 7.0 with 1 N hydrochloric acid and with 0-15 M sodium phosphate buffer pH 7.0 (flow rate 50 ml/I5 min). The perfusates were boiled, neutralised, frozen, and stored at

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